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This investigation expanded and refined a model of resistance to persuasion developed by Burgoon, Cohen, Miller, and Montgomery (1978). It is argued that a logical shortcoming of this model of resistance to persuasion is its failure to incorporate the notion of confirmation and disconfirmation of receiver expectations. Support was found for the prediction that violations of induced receiver expectations and the intensity of a persuasive message are mediators of resistance to persuasion. Positive violations of expectations induce counterarguing and lead to reversals of initial positive attitudes after receipt of a second message arguing on the same side of an attitude issue. Negative violations of receiver expectations decrease the probability of counterarguing, and increase the vulnerability of people to subsequent persuasive attacks. Strong support for the predictions was obtained in this investigation. Competing explanations for the results were ruled out through the utilization of a counterbalanced design and control procedures. These results provide a partial replication of the earlier empirical evidence supporting this new model of resistance to persuasion and cannot be explained by other models of resistance to persuasion. Moreover, the findings break new theoretical ground in their explanation of findings that appear counterintuitive without reference to this theoretical rationale.

Lysergic acid amide and isolysergic acid amide have been extracted and isolated from the seed of Hawaiian baby wood rose. The ergoline alkaloids were identified by TLC, melting point determination, and UV and IR spectrophotometry.

Integration of reverse transcribed retroviral cDNA is not restricted to particular host DNA sequences. However, the frequency of integration into a particular phosphodiester bond is influenced by the local sequence. Here we examine the target-sequence preferences of purified HIV integrase and viral nucleoprotein complexes (preintegration complexes) isolated from freshly infected cells. We find that the three-base sequence including the integration site is not the major factor determining the frequency of integration, since identical triplets embedded in different sequences are used with very different efficiencies. However, there is a statistically significant bias against integration upstream of a pyrimidine nucleotide. The target-sequence preferences of purified integrase and preintegration complexes are very different. Strong integration sites on opposite DNA strands occur in pairs separated by five residues when preintegration complexes are used but not with purified integrase. These studies highlight the difference between the two sources of HIV integration activity and may provide the basis for a simple assay for the correct assembly of viral nucleoprotein complexes.

In this paper, we extend a result of Joseph and Finkelstein and show that there is no group G such that G' is an extra-special p-group of exponent > p (p odd). K. Joseph and L. Finkelstein [2] have shown that if p is an odd prime, there does not exist a finite group G satisfying the following three conditions: (i) G' is an extra-special p-group of exponent > p. (ii) Z (G ) C G'. (iii) G acts irreducibly on G'/Z(G'). It is the object of this paper to prove that their result remains valid even if conditions (ii) and (iii) are dropped. That is, there is no finite group G such that G' is an extra-special p-group of exponent > p (p odd). Recall that a finite p-group G is called extra-special if Z(G) = G', and IG'l = p. We now list a series of lemmas which will be needed for the main theorem. In all that follows, p is an odd prime. LEMMA 1. Let G be an extra-special p-group. Then (a) (xy)P = xPyP, (b)xP E Z(G)for all x,y E G. PROOF. See [1, p. 183]. LEMMA 2. Let G be an extra-special p-group of exponent > p, and let U = {x E GlxP = 1}. Then U is a characteristic subgroup of G and [G: U] = P. PROOF. The fact that U is a characteristic subgroup follows immediately from Lemma l(a), and the fact that automorphisms preserve order. The map x -* xP is a homomorphism of G onto Z(G) with kernel U. Hence G/U Z(G) and [G: U] = p. LEMMA 3. Let G be a finite p-group of linear transformations acting on a vector space V over a field F of characteristic p. Then some nonzero vector of V is fixed by every element of G. PROOF. See [ 1, p. 3 1]. LEMMA 4. Suppose an abelian group G acts as a group of linear transformations Received by the editors August 15, 1975. AMS (MOS) subject classifications (1970). Primary 20F35. ?D American Mathematical Society 1976

Behavioral medicine is a new and still evolving concept in the health care field. As noted elsewhere (Gentry, 1982), the term itself has been used in several distinct ways to highlight teaching, research, and clinical service activities of various groups of behavioral, social, and biomedical scientists and clinicians. The two primary tracks of activities that fall under this rubric essentially have to do with: (a) the application of “behaviorism” to medicine, and (b) an integration of thought and technology between biomedical and behavioral science disciplines. The former represents an outgrowth of Birk’s (1973) initial use of the term in defining the merits of biofeedback in treating medical disorders such as asthma, epilepsy, tension and migraine headaches, and Raynaud’s Disease. The latter reflects a consensus definition emanating from the now historic Yale Conference on Behavioral Medicine (Schwartz & Weiss, 1978b) and subsequently amended at a similar meeting held at the Institute of Medicine, National Academy of Sciences (Schwartz & Weiss, 1978a).

Transcatheter electrocoagulation (TCEC) was used for vessel occlusion in combination with embolization by Gelfoam and/or Ivalon in six patients in whom other interventional or surgical techniques were considered dangerous or unfeasible. The technique was effective in decreasing or obliterating the blood supply to variously located lesions in all cases. The only complications were small skin burns in one patient and a small ulceration of the upper lip in another.

Transcatheter electrocoagulation is an effective method of experimental vessel occlusion even in the presence of thrombocytopenia and heparinization. This technique was used to occlude 13 arteries in 3 patients. In vitro testing suggests that intra-arterial bipolar platinum electrodes may achieve the therapeutic objectives more rapidly and with less risk, but more investigative work is required.

Permanent post-traumatic dislocation of the patella is an extremely rare condition, and is often confused with congenital dislocation. The anatomic abnormalities differ in the two conditions: in the former there is an adaptive flattening of the patella, in the latter there is a propensity for flexion contractures and incongruity of the patella and trochlea. Treatment options include observation, patellar realignment, and patellectomy. In the patient reported, surgical correction appeared to result in patellar alignment.

Several recent protein crystallographic structure determinations have demonstrated the existence of considerable tertiary structural similarity among proteins otherwise having little similarity in either amino acid sequence or biological function. In order to assess the possibility that such proteins may have arisen through processes of divergent evolution from a common ancestor, a graphical presentation is given which correlates the pattern of allowed single base substitutions defined by the genetic code with the associated changes in the structural properties of the encoded amino acids. The results show that while a large degree of structural conservation is evident due to codon synonomy, there is, in general, little tendency for the code to be structurally conservative in the majority of the cases where codon single-base changes result in amino acid substitutions. The possible consequences of this pattern of potential amino acid substitutions are discussed in relation to protein evolutionary processes.

The five cases of atlanto-occipital dislocation reported in the world literature are reviewed, and four additional cases are presented, including two survivors. The pathological anatomy of this potentially catastrophic injury and its management are briefly discussed. Because immediate recognition of the atlanto-occipital dislocation is critical to proper treatment and because the neurological findings are extremely varied, a new radiographic criterion for its identification has been developed.

Whereas previously the output of HIV resistance tests has been based on therapeutically arbitrary criteria, there is now an ongoing move towards correlating test interpretation with virological outcomes on treatment. This approach is undeniably superior, in principle, for tests intended to guide drug choices. However the predictive accuracy of a given stratagem that links genotype or phenotype to drug response is strongly influenced by the study design, data capture and analytical methodology used to derive it. For genotyping, the most widely used resistance tool in clinical practice, these considerations are further complicated by the range of mutational patterns present in the treated population. There is no definitively superior methodology for generating a genotype-response association for use in interpreting a resistance test, and the various approaches used to date all have their strengths and weaknesses. This review discusses the processes involved in constructing such tools, with particular emphasis on establishing validated mutation score rules, and examines the key issues and confounding factors that influence predictive accuracy outside the originating dataset. Since the size of the sample is a key influence on the statistical power to determine an effect, it is hoped that a greater understanding of the influence of study design and methodology will assist the development of standardized outcome measures and reporting formats that allow data pooling at the international level.

In most European countries, HIV drug resistance testing has become a routine clinical tool. However, its practical implementation in a clinical context is demanding. The European HIV Drug Resistance Panel was established to make recommendations to clinicians and virologists on this topic and to propose quality control measures. The panel recommends resistance testing for the following indications: i) drug-naive patients with acute or recent infection; ii) therapy failure, including suboptimal treatment response, when treatment change is considered; iii) pregnant HIV-1-infected women and paediatric patients with detectable viral load when treatment initiation or change is considered; and iv) genotype source patient when post-exposure prophylaxis is considered. In addition, for drug-naive patients with chronic infection in whom treatment is to be started, the panel suggests that resistance testing should be strongly considered and recommends testing the earliest sample for drug resistance if suspicion of resistance is high or prevalence of resistance in this population exceeds 10%. The panel does not favour genotyping over phenotype, however it is anticipated that genotyping will be used more often because of its greater accessibility, lower cost and faster turnaround time. For the interpretation of resistance data, clinically validated systems should be used to the greatest extent possible. It is mandatory that laboratories performing HIV resistance tests take regular part in quality assurance programs. Similarly, it is necessary that HIV clinicians and virologists take part in continuous education and meet regularly to discuss problematic clinical cases. Indeed, resistance test results should be used in the context of all other clinically relevant information for predicting therapy response. The panel also encourages the timely collection of epidemiological information to estimate the impact of transmission of resistant HIV and the prevalence of HIV-1 non-B subtypes in the different European countries. ispartof: Antiviral therapy vol:9 issue:6 pages:829-848 ispartof: location:England status: published

Antiretroviral therapy for HIV infection requires life-long access and strict adherence to regimens that are both expensive and associated with toxicities. There is growing recognition that a curative intervention will be needed to fully stop the epidemic. The failure to eradicate HIV infection during long-term antiretroviral therapy reflects the intrinsic stability of the viral genome in latently infected CD4+ T cells and other cells and perhaps ongoing low-level viral replication. Heterogeneity in latently infected cell populations and homeostatic proliferation of infected cells may influence the dynamics of virus production and persistence. Chronic immune activation, inflammation and immune dysfunction persist despite potent antiretroviral therapy and likely have important effects on the size and distribution of the viral reservoir. The inability of the immune system to recognize cells harboring latent virus and to eliminate cells actively producing virus represents the biggest challenge to finding a cure. In this perspective, we highlight new approaches toward unraveling the complex virus-host interactions that lead to persistent infection and latency and discuss the rationale for combining novel therapeutic strategies with current antiretroviral treatment options with the goal of curing HIV disease.

THE ASSOCIATION between renal vein thrombosis and the nephrotic syndrome is well documented in the literature. Although some investigators have suggested that renal vein thrombosis precedes the onset of the nephrotic syndrome and hence serves as the initiating event, 1 more recent observations imply that the nephrotic syndrome usually precedes the development of renal vein thrombosis. We report such a progression of events in a patient who had the nephrotic syndrome and in whom idiopathic membranous glomerulonephritis was found on histologic examination of the kidney. Later, renal vein thrombosis complicated the course of the patient's illness. Report of a Case A 54-year-old man was hospitalized with peripheral edema, mild hypertension, and proteinuria of three months' duration. The blood pressure on admission was 150/80 mm Hg, and there was pitting edema (2+) to the level of the knees bilaterally. Results of the remaining aspects of the physical examination were unremarkable. Evaluation

Methods Each study was double-blind and randomized; all pts received a background ART regimen (see table in Figure 1). Primary results have been presented for each study. Protocol (P) 004 in treatment-naive pts was a dose-ranging study of RAL vs. efavirenz (EFV) until week 48 after which all pts in RAL groups received 400 mg BID. BENCHMRK-1 and -2 were identical Phase III studies using RAL at 400 mg BID vs. placebo (PBO) in highly treatment-experienced pts with multi-drug resistant virus failing other therapies. Each of the three studies showed potent clinical efficacy for RAL-treated pts. In this analysis, P004 results are shown for all RAL dose groups combined at week 96, and BENCHMRK-1 and -2 results are shown combined at week 48. Non-B subtypes were combined for the analyses due to small numbers of each specific non-B subtype.